Over the last century the neurocentral junction (NCJ) has been identified as a potential cause of adolescent idiopathic scoliosis (AIS). Disparate growth at this site has been thought to lead to pedicle asymmetry, which then causes vertebral rotation and ultimately, the development of scoliotic curves. The objectives of this study are (1) to incorporate pedicle growth and growth modulation into an existing finite element model of the thoracic and lumbar spine already integrating vertebral body growth and growth modulation; (2) to use the model to investigate whether pedicle asymmetry, either alone or combined with other deformations, could be involved in scoliosis pathomechanisms. The model was personalized to the geometry of a nonpathological subject and used as the reference spinal configuration. Asymmetry of pedicle geometry (i.e. initial length) and asymmetry of the pedicle growth rate alone or in combination with other AIS potential pathogenesis (anterior, lateral, or rotational displacement of apical vertebra) were simulated over a period of 24 months. The Cobb angle and local scoliotic descriptors (wedging angle, axial rotation) were assessed at each monthly growth cycle. Simulations with asymmetrical pedicle geometry did not produce significant scoliosis, vertebral rotation, or wedging. Simulations with asymmetry of pedicle growth rate did not cause scoliosis independently and did not amplify the scoliotic deformity caused by other deformations tested in the previous model. The results of this model do not support the hypothesis that asymmetrical NCJ growth is a cause of AIS. This concurs with recent animal experiments in which NCJ growth was unilaterally restricted and no scoliosis, vertebral wedging, or rotation was noted.

The baseline used to assess adolescent idiopathic scoliosis vertebral morphology must take into consideration the extent and direction of normal vertebral asymmetry. The pattern of vertebral asymmetry seen inadolescent idiopathic scoliosis may depend on the specific cause of the disorder, with no consistent pattern evident when data from different causes are pooled together.

Although MRI underestimated the extent of NCJ closure, MRI accurately showed whether cartilage was present or absent at the NCJ site. MRI determination of the age of NCJ closure appears reliable, and further exploration of the asymmetric growth hypothesis is required.

The normal development of the NCS at the level of individual vertebrae and also along the vertebral column as a whole was determined using MRI. These patterns of development are valuable and necessary to evaluate the role of the NCS in pathological conditions.